Several laboratories, including ours, have demonstrated that chronic exposure to cigarette smoke results in immunosuppression which may be due to effects on both B and T cell function. Preliminary results from our laboratory have further suggested that immunosuppression from cigarette smoking may be related to (a) its effects on antigen-specific lymphocyte signal transduction and, (b) nicotine may be one of the major components of cigarette smoke affecting the immune response. In preliminary experiments, we have shown that lymphocytes from nicotine- treated animals fail to produce the normal AFC response and, following the ligation of antigen receptors in vitro, do not elevate the intracellular calcium levels normally. This suggests that nicotine affects at least one step in the antigen-induced signal transduction pathway preceding the elevation of intracellular calcium. Therefore, one of the subjects of my thesis will be to determine the effects of nicotine on the activity of protein tyrosine kinases (PTKs) and phospholipase C (PLC). The second part of my thesis will be the results from probing mRNA isolated from T and B cells with cDNAs specific for various subunits of nicotinic receptors. This should provide some idea of the type of nicotinic receptors that are present on T and B cells and may explain how in vitro nicotine treatment causes activation of lymphocytes.